Louis Ragolia, PhD

Director, Biomedical Research; Associate Professor

Research

The prevalence of obesity and type 2 diabetes is well-documented and continues to rise in both the United States and worldwide. Bariatric surgery has been shown to be more effective than nonsurgical treatments for sustained weight loss in moderate to severely obese type 2 diabetics. In addition to weight loss, remission of type 2 diabetes is observed in the majority of patients after the two most commonly performed bariatric operations, the Roux-en-Y gastric bypass and the sleeve gastrectomy. This phenomenon is even more remarkable as it occurs within days after surgery, independent of any significant weight loss. While several possible explanations have been proposed, including caloric restriction, malabsorption, and enhanced incretin secretion, the precise mechanism of how bariatric surgery ameliorates diabetes and the long-term effects on the cardiovascular system, is poorly understood.

Recently, we reported accelerated glucose intolerance and atherosclerosis in a genetic knockout (KO) of lipocalin-type prostaglandin D2 synthase (L-PGDS). A growing body of evidence demonstrates a strong association between serum L-PGDS levels and diabetes, hypertension, and cardiovascular disease. We have exciting new data demonstrating that bariatric surgery stimulates L-PGDS expression and bile acid synthesis. Furthermore, we have shown that bariatric surgery is ineffective in reversing diabetes in L-PGDS KO mice. We are expanding on these findings and exploring the precise role of this protein in and bile acid metabolism in the reversal of diabetes-associated cardiovascular complications after bariatric surgery.